2016
DOI: 10.18632/aging.100897
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Abstract: Cellular senescence is a stress response mechanism that limits tumorigenesis and tissue damage. Induction of cellular senescence commonly coincides with an immunogenic phenotype that promotes self-elimination by components of the immune system, thereby facilitating tumor suppression and limiting excess fibrosis during wound repair. The mechanisms by which senescent cells regulate their immune surveillance are not completely understood. Here we show that ligands of an activating Natural Killer (NK) cell recepto… Show more

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Cited by 171 publications
(144 citation statements)
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References 59 publications
(106 reference statements)
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“…The SASP, composed of pro‐inflammatory cytokines, chemokines, growth factors, and proteases, can modulate the senescent cell's microenvironment and promote its interaction with the immune system (Coppe et al , ; Lujambio et al , ; Sagiv & Krizhanovsky, ; Sagiv et al , ). We found that compared to 2‐day cultures, our trophoblast cultures on day 5 indeed exhibited significantly upregulated gene sets associated with the immune response, cytokine activity, and major signaling pathways regulating the SASP, including JAK‐STAT and MAPK (Fig D).…”
Section: Resultsmentioning
confidence: 99%
“…The SASP, composed of pro‐inflammatory cytokines, chemokines, growth factors, and proteases, can modulate the senescent cell's microenvironment and promote its interaction with the immune system (Coppe et al , ; Lujambio et al , ; Sagiv & Krizhanovsky, ; Sagiv et al , ). We found that compared to 2‐day cultures, our trophoblast cultures on day 5 indeed exhibited significantly upregulated gene sets associated with the immune response, cytokine activity, and major signaling pathways regulating the SASP, including JAK‐STAT and MAPK (Fig D).…”
Section: Resultsmentioning
confidence: 99%
“…It is thought the clearance of senescent cells can result from the activity of both adaptive and innate immunity; the latter resulting from the increased expression of ligands (e.g. NKG2D) on senescent cells that target them for selective killing by natural killer (NK) lymphocytes (Sagiv et al, 2016). Therefore, mechanisms to augment cellular immunity or NK function might be therapeutically beneficial in some settings.…”
Section: Translating Senescencementioning
confidence: 99%
“…Drug‐induced transcription of MICA and PVR genes involves the transcriptional factor E2F and is dependent on the cellular redox state . Notably, NKG2D and DNAM‐1 ligands have been shown to be expressed by senescent cells and drug‐induced senescent tumor cells, unmasking an important role of NK cells for the immune surveillance of senescent cells …”
Section: Introductionmentioning
confidence: 99%